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Immune System > Hypersensitivity + Coombs test > Flashcards

Hypersensitivity + Coombs test Flashcards

1
Q

Define Hypersensitivity

A

Antigen-specific immune responses that are either Inappropriate or Excessive and result in Harm to Host

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2
Q

What are the 2 types of triggers of Hypersensitivity?

A
  • Exogenous Antigens (infectious microbes, Drugs, Non infectious substances)
  • Intrinsic Antigens (Self antigens, infectious microbes)
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3
Q

List and describe the 4 broad types of Hypersensitivity reactions

A

Type I: Immediate Allergy (IgE driven, mast cell degradanulation)

Type II: Antibody mediated

Type III: Immune complex mediated

Type IV: Cell mediated- Delayed

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4
Q

What are the 2 phases of Hypersensitivity reactions?

A

Sensitisation phase;
- First encounter with antigen, Activation of APCs and Memory effector cells

Effector phase;
- Pathological reaction upon re-exposure to same antigen

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5
Q

List 5 treatments for Type I Hypersensitivity reactions

A
  • Allergen desensitisation
  • Anti-IgE antibodies
  • Antihistamine
  • LTRA
  • Corticosteroids
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6
Q

For Type II Hypersensitivity reactions, state the;

  • Time taken to develop
  • Antibodies involved
  • Targets
A
  • Develops within 5-12 hours
  • Involves IgM/ IgG antibodies
  • Targets are cell surface antigens

(Exogenous cell surface antigens: A/B, Rhesus D antigens)
(Endogenous cell surface antigens: Self antigens)

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7
Q

What are 2 different types of outcomes of a Type II Hypersensitivity reaction

A
  • Tissue/ cell damage

- Physiological change

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8
Q

List the 2 mechanisms that can lead to Tissue/ Cell damage in a Type II Hypersensitivity reaction

A
  • Complement activation

- Antibody-dependent cell cytotoxicity (Natural Killer cells)

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9
Q

List the 3 processes involved in Complement Activation

A
  • Cell lysis
  • Neutrophil recruitment/ activation
  • Opsonisation
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10
Q

List 7 Type II Hypersensitivity reactions

A
  • ABO Transfusion reaction
  • Haemolytic Disease of the Newborn (HDN)
  • Graves’
  • Autoimmune Haemolytic Anaemia
  • Myasthenia Gravis
  • Goodpasture’s
  • Immune Thrombocytopenic Purpura
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11
Q

Which blood groups are universal PLASMA and BLOOD donors?

A

PLASMA: AB (lack A and B antibodies)

BLOOD: O (lack A or B antigens)

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12
Q

Describe the immune mechanism of ABO/ Haemolytic Transfusion Reactions

A
  • Incompatibility in ABO or Rhesus D antigens
  • Donor RBC destroyed by Recipient’s Immune system
  • RBC lysis induced by Type II Hypersensitivity, involving natural IgM antibodies
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13
Q

List 4 consequences of ABO/ Haemolytic Transfusion reaction

A
  • Shock
  • Kidney failure
  • Circulatory collapse
  • Death
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14
Q

What does Rh (+ve) blood mean?

A

Presence of D antigen on RBCs

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15
Q

Describe the immune mechanism of Haemolytic Disease of the Newborn (HDN)

A
  • In Rh (-ve) pregnant woman, baby carries Rh (+ve) blood, so small amounts of D-positive RBCs enter maternal circulation
  • Mother produces anti-D IgG antibodies. In future pregnancies, these IgG ABs cross Placenta
  • Maternal anti-D IgGs attach to foetal RBCs if they are Rh (+ve)
  • RBCs with attached ABs are cleared by Liver and Spleen macrophages
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16
Q

How is HDN prevented?

A

Rh (-ve) pregnant women are given a small amount of Rh Immunoglobulin/ RhoGAM.

This prevents formation of their own anti-D antibodies

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17
Q

Describe the clinical features of a baby born with HDN

A
  • RBC destruction causes elevation of Bilirubin in Foetal blood
  • After birth Bilirubin is no longer cleared by Placenta, so Bilirubin accumulates-> Jaundice
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18
Q

What is the main complication of increased Bilirubin levels for the baby?

A
  • Bilirubin may enter the brain to cause Kernicterus.

- This can be fatal and leaves permanent neurological damage in surviving babies

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19
Q

Why does an ABO mismatch rarely cause HDN?

A

The naturally occurring Anti-A/ Anti-B antibodies are IgM, so DO NOT cross the placenta

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20
Q

List the 2 mechanisms that can lead to Physiological Change in a Type II Hypersensitivity reaction?

For each mechanism, suggest a disease that it causes

A

Receptor stimulation;

  • Graves’ disease
  • (Increased thyroid activity, Antigen= TSH receptor)

Receptor blockade;

  • Myasthenia Gravis
  • (Impaired neuromuscular signalling, Antigen= AChR)
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21
Q

List 4 therapeutic approaches to Tissue/ Cell damage in a Type II Hypersensitivity reaction

A
  • Anti-inflammatory drugs (complement activation)
  • Plasmapheresis (ABs and inflammatory mediators)
  • Splenectomy (Opsonisation/ phagocytosis)
  • IV Immunoglobulin/ IVIG (IgG Degradation)
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22
Q

Suggest 2 therapeutic approaches to Physiological change in a Type II Hypersensitivity reaction

A
  • Correct metabolism (for receptor stimulation e.g antithyroid drugs)
  • Replacement therapy (for receptor blockade e.g Pyridostigmine in Myasthenia Gravis)
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23
Q

For Type III Hypersensitivity, state the;

  • Time taken to develop
  • Antibodies involved
  • Targets
  • Cause of tissue damage
A
  • Develops in 3-5 hours
  • Immune complexes (between antigens and IgM/IgG)
  • Targets soluble antigens (Foreign or Endogenous)
  • Deposition of immune complexes in tissues
24
Q

List 3 key factors that affect Immune Complex pathogenesis in Type III Hypersensitivity

A
  • Complex size (Small+large ICs cleared easily, Intermediate ICs very hard to clear)
  • Host response (Low affinity antibody, Complement deficiency)
  • Local tissue factors (Haemodynamic and Physiochemical factors)
25
Q

In Type III Hypersensitivity, persistence of Immune Complex deposition drives the disease.

List 4 common systems affected

A
  • Joints
  • Skin
  • Small vessels
  • Kidney
26
Q

List 3 diseases caused by Type III Hypersensitivity

A
  • RA (Antigen= Anti-rheumatoid Factor IgG/ Fc portion of IgG)
  • Glomerulonephritis (Infectious)
  • Lupus/ SLE (Antigen= dsDNA, more common in Females, can cause repeated miscarriages)
27
Q

Describe the immune mechanism of a Type III Hypersensitivity reaction

A
  1. Intermediate ICs deposited in tissue
  2. Complement activated
  3. Neutrophil chemotaxis
  4. Neutrophil adherence and degranulation
28
Q

For Type IV Hypersensitivity, state the;

  • Time taken to develop
  • Antibodies involved
  • 3 types of response to Exogenous antigens
A
  • Develops within 24-72 hours
  • Involves Lymphocytes and Macrophages (TH1 cells)

Three types;

  • Contact Hypersensitivity
  • Tuberculin Hypersensitivity
  • Granulomatous Hypersensitivity
29
Q

Describe the duration and outcome of Type IV Contact Hypersensitivity

A

Duration: 48-72 hours
Outcome: Epidermal reaction

30
Q

Describe the duration and outcome of Type IV Tuberculin Hypersensitivity

A

Duration: 48-72 hours
Outcome: Dermal reaction (Induration and swelling)

31
Q

Describe the duration and outcome of Type IV Granulomatous Hypersensitivity

List 4 examples

A

Duration: 21-48 days
Outcome: Tissue damage

  • Sarcoidosis
  • TB
  • Leprosy
  • Schistosomiasis
32
Q

List 3 diseases caused by a Type IV Hypersensitivity response to Endogenous antigens

A
  • RA
  • Hashimoto’s
  • Insulin dependent DM (Type 1)
33
Q

Describe the treatment options for Type III and IV Hypersensitivity

A
  • Monoclonal antibodies

Anti-inflammatory drugs;

  • NSAIDs
  • Corticosteroids
  • Steroid sparing agents (Azathioprine, Mycophenolate Mofetil, Cyclophosphamide)
34
Q

Which drug is used to treat Myasthenia Gravis and how does it work?

A

Pyridostigmine: Is an AChesterase Inhibitor, so increases synaptic concentration of ACh.

This prolongs the action of ACh, so greater chance of APs ocuring the muscle, leading to contraction

35
Q

Type I Hypersensitivity is Allergy. Compare the 2 types of Immediate Reaction

A

Local: Ingested/ inhaled antigen

Systemic: Insect sting/ IV administration

(Allergens are environmental, non-infectious agents)

36
Q

List the 3 types of allergen exposure

A
  • Seasonal (pollen)
  • Perennial (throughout year) (animal dander, dust mite)
  • Accidental (Insect venom, Drugs, Chemicals, Food)
37
Q

Describe the 2 mechanisms of Type I Hypersensitivity

A
  • Mast cell activation

Abnormal adaptive response against allergen’

  • Activation of TH2 cells
  • Release of IL-4, IL-5, IL-13
  • IgE production
38
Q

Development of allergy can be influenced by Genetics and Environmental Exposure.

What are 2 reasons allergies are more prevalent in developed countries?

A
  • Reduced infection burden

- Microbial Dysbiosis (Alteration of the symbiotic relationships with parasites and bacteria)

39
Q

What is the Hygiene Hypothesis?

A

Children exposed to animals, pets and microbes in the early post-natal period appear to be protected against certain allergic diseases

40
Q

Describe the strategic location of Mast cells

A
  • In most Mucosal and Epithelial tissues (GI, Skin, Respiratory epithelium)
  • In Connective Tissue surrounding RBCs
41
Q

List 5 Mast cell mediators

A
  • Tryptase (Remodels CT matrix)
  • Histamine
  • Platelet Activating Factor
  • Leukotrienes (C4, D4, E4)
  • Interleukins 4,5,13
42
Q

State the biological effects of Histamine and Leukotrienes

A
  • Increased vascular permeability

- Cause smooth muscle contraction

43
Q

State the biological effects of Platelet Activating Factor

A
  • Attracts Leukocytes

- Activates Neutrophil, Eosinophils and Platelets

44
Q

Describe the immune mechanism of allergic reaction

A
  1. 1st exposure to allergen;
    - TH2 response and allergen-specific IgE produced
    - Allergen-specific IgE binds to Mast cell via FcεRI (high affinity IgE receptor)
  2. 2nd exposure;
    - Allergen will cross link with 2 IgEs
    - Causes activation of Mast Cells-> Degranulation
45
Q

Describe Mast cell degranulation (mediators released and biological effects)

A
  • Release of Histamine and Leukotrienes

Causes;

  • Increased vascular permeability
  • Vasodilation
  • Bronchial constriction
46
Q

What causes Urticaria?

What are the mediators involved?

A
  • Mast cell activation in Epidermis

- Histamine and Leukotrienes/ Cytokines

47
Q

With prolonged + chronic exposure, what can Urticaria develop into?

A
  • Atopic dermatitis

- Eczema

48
Q

What causes Angioedema?

What mediators are involved?

A
  • Mast cell activation in deep dermis

- Histamine and Bradykinin

49
Q

List 5 systemic effects of Mast cell activation (Anaphylaxis)

A
  • Hypotension
  • CVS collapse
  • Generalised Urticaria
  • Breathing problems
  • Angioedema
50
Q

State the treatment of Anaphylactic shock and list ways it helps

A
  • IM Adrenaline (absorbed, works better than SC)
  • Reverses peripheral vasodilation, Reduces oedema, Alleviates hypotension
  • Reverses Airway Obstruction/ Bronchospasm
  • Increases the force of Myocardial Contraction
  • Inhibits Mast cell activation
51
Q

When treating Anaphylaxis, how many adrenaline doses are needed?

A

May need multiple

52
Q

Of the 5 available therapies for Type I Hypersensitivity, which 3 target Mast cel activation

A
  • Antihistamines
  • LTRAs
  • Corticosteroids
53
Q

What are the 2 types of Coombs test?

A
  • Direct Coombs test/ Direct Antiglobulin test (DAT)

- Indirect Coombs test/ Indirect Antiglobulin test (IAT)

54
Q

Compare the uses of the Direct and Indirect Coombs test

A

DAT;

  • Looks directly at RBCs
  • Used to detect Autoimmune Haemolytic Anaemia

IAT;

  • Looks at plasma
  • Used to check Compatibility of Donor blood AND to see if maternal blood contains ABs that may harm baby
55
Q

How does the Direct Coombs test work?

A

Positive result if Coombs’ Reagent ABs bind to ABs that are already attached to RBC antigens

56
Q

How does the Indirect Coombs test work?

A

Looks for unattached ABs in plasma

Immune System (4 decks)

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